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백재승,김시황,김혜원,정명희,김명석,Paick, Jae-Seung,Kim, Si-Whang,Kim, Hae-Won,Chung, Myung-Hee,Kim, Myung-Suk The Korean Society of Pharmacology 1985 대한약리학잡지 Vol.21 No.1
항균제 nitrofurantion에 의한 폐독작용의 생화학적 기전을 규명하기 위한 연구 일환으로 in vitro에서 폐장 microsome 지질의 과산화 및 반응성 산소 radical $(O^{-}_{2}{\cdot},\;H_2O_2,\;OH{\cdot},\;^1O_2)$의 생성에 대한 nitrofurantion의 영향과 양자 간의 상호 관련성을 검토하였다. Nitrofurantion은 호기성 반응 조건에서 돼지 폐장 microsome의 NADPH 의존성 지질 과산화를 용량 의존적으로 증가시킬 뿐 아니라 $O^{-}_{2}{\cdot},\;H_2O_2$ 및 두 radical의 상호 작용으로 2차적으로 형성되는 $OH{\cdot}$의 생성 또한 촉진하였으며 $^1O_2$생성은 관찰되지 않았다. 이와 같은 폐장 microsome지질 과산화 증가는 SOD 및 catalase에 의하여 억제될 뿐만 아니라 $OH{\cdot}$ 제거 물질인 mannitol, thiourea에 의하여도 현저히 억제되었으며, $^1O_2$ 제거 물질에 의하여는 영향을 받지 않았던 한편 염기성 반응 조건에서는 nitrofurantoin에 의한 지질 과산화가 관찰되지 않았다. 이상의 결과로 미루어 보아 nitrofurantoin은 폐장 microsome의 NADPH 의존적이 반응성산소 radical $(O^{-}_{2}{\cdot},\;H_2O_2$ 및 $OH{\cdot})$의 생성을 증가시키며 이들 중 특히 $OH{\cdot}$ 에 의한 microsome막 지질 과산화를 촉진하는 것으로 결론지었고, 이와 같은 in vivo 현상은 nitrofurantion의 in vitro 폐독작용의 기전을 설명하는 일부가 될 것으로 사료하였다. In vitro effects of nitrofurantoin, an antimicrobial agent for acute and chronic urinary tract infection, on the lung microsomal lipid peroxidation and the generation of reactive oxygen radicals were investigated to elucidate the biochemical mechanisms of its in vivopulmonary toxicity. The interaction of nitrofurantoin with porcine lung microsome resulted in significant lipid peroxidation. In addition, nitrofurantoin stimulated the generation of reactive oxygen radicals, $O^{-}_{2}{\cdot},\;H_2O_2$ as well as a highly reactive secondary oxygen species, $OH{\cdot}$. The stimulation of lipid peroxidation was inhibited not only by superoxide dismutase and catalase, but also by hydroxyl radical scavengers, mannitol and thiourea. Neither singlet oxygen $({^1}O_{2})$ was detected during the incubation of microsome with nitrofurantoin, nor lipid peroxidation was inhibited by singlet oxygen scavengers. When incubated anaerobically under the nitrogen atmosphere, the ability of nitrofurantoin to stimulatle lipid peroxidation was abolished. It appears that NADPH-dependent metaboliam of nitrofurantoin in pulmonary microsome under aerobic condition is accompanied by the stimulation of lipid peroxidation through the mediation of reactive oxygen radicals, particularly hydroxyl radical. It is strongly suggested from these results that the stimulation of pulmonary microsomal lipid peroxidation by the reactive oxygen radical may be a in vivo mechanism of pulmonary toxicity caused by nitrofurantoin.
Nitrofurantion이 폐장 미크로솜 지질과산화와 반응성 산소 라디칼 생성에 미치는 영향
백재승(Jae-Seung Paick),김시황(Si-Whang Kim),김혜원(Hae-Won Kim),정명희(Myung-Hee Chung),김명석(Myung-Suk Kim) 대한약리학회 1985 대한약리학잡지 Vol.21 No.1
항균제 nitrofurantion에 의한 폐독작용의 생화학적 기전을 규명하기 위한 연구 일환으로 in vitro에서 폐장 microsome 지질의 과산화 및 반응성 산소 radical (O<sub>2</sub><sup>-</sup>⋅, H<sub>2</sub>O<sub>2</sub>, OH⋅, <sup>1</sup>O<sub>2</sub>)의 생성에 대한 nitrofurantion의 영향과 양자 간의 상호 관련성을 검토하였다. Nitrofurantion은 호기성 반응 조건에서 돼지 폐장 microsome의 NADPH 의존성 지질 과산화를 용량 의존적으로 증가시킬 뿐 아니라 O<sub>2</sub><sup>-</sup>⋅, H<sub>2</sub>O<sub>2</sub> 및 두 radical의 상호 작용으로 2차적으로 형성되는 OH⋅의 생성 또한 촉진하였으며 <sup>1</sup>O<sub>2</sub>생성은 관찰되지 않았다. 이와 같은 폐장 microsome지질 과산화 증가는 SOD 및 catalase에 의하여 억제될 뿐만 아니라 OH⋅ 제거 물질인 mannitol, thiourea에 의하여도 현저히 억제되었으며, <sup>1</sup>O<sub>2</sub> 제거 물질에 의하여는 영향을 받지 않았던 한편 염기성 반응 조건에서는 nitrofurantoin에 의한 지질 과산화가 관찰되지 않았다. 이상의 결과로 미루어 보아 nitrofurantoin은 폐장 microsome의 NADPH 의존적이 반응성산소 radical (O<sub>2</sub><sup>-</sup>⋅, H<sub>2</sub>O<sub>2</sub> 및 OH⋅)의 생성을 증가시키며 이들 중 특히 OH⋅ 에 의한 microsome막 지질 과산화를 촉진하는 것으로 결론지었고, 이와 같은 in vivo 현상은 nitrofurantion의 in vitro 폐독작용의 기전을 설명하는 일부가 될 것으로 사료하였다. In vitro effects of nitrofurantoin, an antimicrobial agent for acute and chronic urinary tract infection, on the lung microsomal lipid peroxidation and the generation of reactive oxygen radicals were investigated to elucidate the biochemical mechanisms of its in vivopulmonary toxicity. The interaction of nitrofurantoin with porcine lung microsome resulted in significant lipid peroxidation. In addition, nitrofurantoin stimulated the generation of reactive oxygen radicals, O<sub>2</sub><sup>-</sup>⋅, H<sub>2</sub>O<sub>2</sub> as well as a highly reactive secondary oxygen species, OH⋅. The stimulation of lipid peroxidation was inhibited not only by superoxide dismutase and catalase, but also by hydroxyl radical scavengers, mannitol and thiourea. Neither singlet oxygen (<sup>1</sup>O<sub>2</sub>) was detected during the incubation of microsome with nitrofurantoin, nor lipid peroxidation was inhibited by singlet oxygen scavengers. When incubated anaerobically under the nitrogen atmosphere, the ability of nitrofurantoin to stimulatle lipid peroxidation was abolished. It appears that NADPH-dependent metaboliam of nitrofurantoin in pulmonary microsome under aerobic condition is accompanied by the stimulation of lipid peroxidation through the mediation of reactive oxygen radicals, particularly hydroxyl radical. It is strongly suggested from these results that the stimulation of pulmonary microsomal lipid peroxidation by the reactive oxygen radical may be a in vivo mechanism of pulmonary toxicity caused by nitrofurantoin.
尿路感染症에 대한 Aminosidine Sulfate(Gabbromicina)의 臨床報告
金時煌,崔樂圭,朱槿源 中央醫學社 1974 中央醫學 Vol.26 No.2
The effects of Aminosidine sulfate in the treatment of urinary tract infections were evaluated in the Dept. of Urology, Seoul National University Hospital from May 1 to September 30, 1973. Fifteen cases of acute gonococcal urethritis, 5 cases of acute non-gonococcal urethritis, 8 cases of acute cystitis and 5 cases of acute pyelonephritis were subjected in this study. All cases were injected 1 gm of Aminosidine sulfate intramuscularly and the treatment period was 3-10 days according to the responses of the drug to the diseases. The success of treatment were based on the subsidence of subjective symptoms. and negative bacteriological study at least until 7 to 10 days after treatment. The cure rate was 86.7% for N. gonorrhea, 100% for staphylococcus aureus, 92.3% for E. coli and 50% for no organism(acute non-gonococcal urethritis), and overall cure rate was 86.7%. No particular side effects or reactions were observed during Aminosidine treatment except severe pain on injection site in 10 cases.
金時煌,李鎭夏,洙槿源 中央醫學社 1973 中央醫學 Vol.24 No.4
The efficacy of Trobicin in the treatment of gonorrhea was evaluated in the Department of Urology, Seoul National University Hospital from October 1, 1972 to January 31, 1973. Seventy five cases of acute gonorrhea in both sex were subjected in this study. Fifty five cases were returned for the follow-up study, 48 hours and 7 days after the injection. A single dose of Trobicin 2.0gm. I. M. was given to all patients who were confirmed as gonorrhea by Gram stain and bacterial culture in chocolate media. The success was assessed by subsidence of subjective symptoms and bacteriological study in the 7 days after the treatment. The cure rate was 95.7% in male and 87.5% in female and the overall cure rate of Torbicine was 94.5% in acute gonorrhea. No particular side effects or reactions were observed except mild pain on injection site. It is considered that Trobicin is one of the most effective drugs in the treatment of acute gonorrhea and a single injection of Trobicin 2. 0 gm. in both sex offers a suitable alternative to penicillin in the treatment of acute gonorrhea.